Machado B H, de-Oliveira M
Departamento de Fisiologia, Universidade de São Paulo, Ribeirão Preto, Brasil.
Braz J Med Biol Res. 1996 Jan;29(1):47-51.
Sino-aortic deafferentation (SAD) in rats produces arterial pressure lability (APL) whose mechanisms are not completely understood. In the present study we infused nifedipine (500 micrograms kg-1 min-1) for 30 min into sham-operated and acute SAD rats (24 h) and the changes in mean arterial pressure (MAP) and APL were measured during this period by a computerized technique. APL was reported as the standard deviation of the mean of all MAP sampling points. In SAD rats with high basal APL levels (SAD high APL, N = 8) nifedipine produced a significant reduction in MAP (from 116 +/- 5 to 88 +/- 3 mmHg) and APL (from 19.62 +/- 1.46 to 9.51 +/- 0.88 mmHg), while in SAD rats with low basal APL levels (SAD low APL, N = 8) it significantly reduced MAP (from 120 +/- 7 to 95 +/- 6 mmHg) and did not change APL (9.46 +/- 0.69 to 10.93 +/- 1.62). Nifedipine infusion into sham-operated rats (N = 8) produced no significant changes in MAP (105 +/- 3 vs 104 +/- 2 mmHg) or APL (4.17 +/- 0.53 vs 3.99 +/- 0.67 mmHg). Since nifedipine infusion reduced APL only in SAD high APL rats but reduced the MAP in both groups of SAD rats, we conclude that its effect on APL is not related to decreases in MAP. These data suggest that extracellular calcium influx through calcium channels plays an important role in the generation of APL, especially in SAD rats with high APL levels.
